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The β Subunit Increases the Ca(2+) Sensitivity of Large Conductance Ca(2+)-activated Potassium Channels by Retaining the Gating in the Bursting States
Coexpression of the β subunit (K(V),(Ca)β) with the α subunit of mammalian large conductance Ca(2+)- activated K(+) (BK) channels greatly increases the apparent Ca(2+) sensitivity of the channel. Using single-channel analysis to investigate the mechanism for this increase, we found that the β subuni...
Autores principales: | , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
1999
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2222905/ https://www.ncbi.nlm.nih.gov/pubmed/10051518 |
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author | Nimigean, Crina M. Magleby, Karl L. |
author_facet | Nimigean, Crina M. Magleby, Karl L. |
author_sort | Nimigean, Crina M. |
collection | PubMed |
description | Coexpression of the β subunit (K(V),(Ca)β) with the α subunit of mammalian large conductance Ca(2+)- activated K(+) (BK) channels greatly increases the apparent Ca(2+) sensitivity of the channel. Using single-channel analysis to investigate the mechanism for this increase, we found that the β subunit increased open probability (P (o)) by increasing burst duration 20–100-fold, while having little effect on the durations of the gaps (closed intervals) between bursts or on the numbers of detected open and closed states entered during gating. The effect of the β subunit was not equivalent to raising intracellular Ca(2+) in the absence of the beta subunit, suggesting that the β subunit does not act by increasing all the Ca(2+) binding rates proportionally. The β subunit also inhibited transitions to subconductance levels. It is the retention of the BK channel in the bursting states by the β subunit that increases the apparent Ca(2+) sensitivity of the channel. In the presence of the β subunit, each burst of openings is greatly amplified in duration through increases in both the numbers of openings per burst and in the mean open times. Native BK channels from cultured rat skeletal muscle were found to have bursting kinetics similar to channels expressed from alpha subunits alone. |
format | Text |
id | pubmed-2222905 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1999 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-22229052008-04-21 The β Subunit Increases the Ca(2+) Sensitivity of Large Conductance Ca(2+)-activated Potassium Channels by Retaining the Gating in the Bursting States Nimigean, Crina M. Magleby, Karl L. J Gen Physiol Article Coexpression of the β subunit (K(V),(Ca)β) with the α subunit of mammalian large conductance Ca(2+)- activated K(+) (BK) channels greatly increases the apparent Ca(2+) sensitivity of the channel. Using single-channel analysis to investigate the mechanism for this increase, we found that the β subunit increased open probability (P (o)) by increasing burst duration 20–100-fold, while having little effect on the durations of the gaps (closed intervals) between bursts or on the numbers of detected open and closed states entered during gating. The effect of the β subunit was not equivalent to raising intracellular Ca(2+) in the absence of the beta subunit, suggesting that the β subunit does not act by increasing all the Ca(2+) binding rates proportionally. The β subunit also inhibited transitions to subconductance levels. It is the retention of the BK channel in the bursting states by the β subunit that increases the apparent Ca(2+) sensitivity of the channel. In the presence of the β subunit, each burst of openings is greatly amplified in duration through increases in both the numbers of openings per burst and in the mean open times. Native BK channels from cultured rat skeletal muscle were found to have bursting kinetics similar to channels expressed from alpha subunits alone. The Rockefeller University Press 1999-03-01 /pmc/articles/PMC2222905/ /pubmed/10051518 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Article Nimigean, Crina M. Magleby, Karl L. The β Subunit Increases the Ca(2+) Sensitivity of Large Conductance Ca(2+)-activated Potassium Channels by Retaining the Gating in the Bursting States |
title | The β Subunit Increases the Ca(2+) Sensitivity of Large Conductance Ca(2+)-activated Potassium Channels by Retaining the Gating in the Bursting States |
title_full | The β Subunit Increases the Ca(2+) Sensitivity of Large Conductance Ca(2+)-activated Potassium Channels by Retaining the Gating in the Bursting States |
title_fullStr | The β Subunit Increases the Ca(2+) Sensitivity of Large Conductance Ca(2+)-activated Potassium Channels by Retaining the Gating in the Bursting States |
title_full_unstemmed | The β Subunit Increases the Ca(2+) Sensitivity of Large Conductance Ca(2+)-activated Potassium Channels by Retaining the Gating in the Bursting States |
title_short | The β Subunit Increases the Ca(2+) Sensitivity of Large Conductance Ca(2+)-activated Potassium Channels by Retaining the Gating in the Bursting States |
title_sort | β subunit increases the ca(2+) sensitivity of large conductance ca(2+)-activated potassium channels by retaining the gating in the bursting states |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2222905/ https://www.ncbi.nlm.nih.gov/pubmed/10051518 |
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